The inflammatory process initiates a localized defense against foreign antigens. The process is characterized by immune activation as well as destruction of nearby tissues secondary to involved release of destructive agents. Initially involved tissue assumes a significant role in provoking the inflammatory response at large (Matzinger, P., The danger model: a renewed sense of self. Science, 2002. 296(5566): p. 301–5; Medzhitov, R. and C. A. Janeway, Jr., Decoding the patterns of self and nonself by the innate immune system. Science, 2002. 296(5566): p. 298–300). One of the primary immunogenic mechanisms triggered by the inflammatory response includes the release of ATP into the extracellular space. ATP is liberated from injured tissue itself—as well as from nearby macrophages, neutrophils, platelets and dying cells—following incidents of stress, infection or other forms of tissue insult (Fredholm, B. B., Purines and neutrophil leukocytes. Gen Pharmacol, 1997. 28(3): p. 345–50; Beigi, R., et al., Detection of local ATP release from activated platelets using cell surface-attached firefly luciferase. Am J Physiol, 1999. 276(1 Pt 1): p. C267–78; Schwiebert, E. M., ABC transporter-facilitated ATP conductive transport. Am J Physiol, 1999. 276(1 Pt 1): p. C1-8; Mizumoto, N., et al., CD39 is the dominant Langerhans cell-associated ecto-NTPDase: modulatory roles in inflammation and immune responsiveness. Nat Med, 2002. 8(4): p. 358–65; Dubyak, G. R. and C. el-Moatassim, Signal transduction via P2-purinergic receptors for extracellular ATP and other nucleotides. Am J Physiol, 1993. 265(3 Pt 1): p. C577–606; Gordon, J. L., Extracellular ATP: effects, sources and fate. Biochem J, 1986. 233(2): p. 309–19). Extracellular ATP can then exert a wide variety of effects on surrounding cells, most notably the induction of apoptotic events leading ultimately to cell death in both lymphocytes and macrophages (Di Virgilio, F., The P2Z purinoceptor: an intriguing role in immunity, inflammation and cell death. Immunol Today, 1995. 16(11): p. 524–8; Gargett, C. E., J. E. Cornish, and J. S. Wiley, ATP, a partial agonist for the P2Z receptor of human lymphocytes. Br J Pharmacol, 1997. 122(5): p. 911–7; Buisman, H. P., et al., Extracellular ATP induces a large nonselective conductance in macrophage plasma membranes. Proc Natl Acad Sci USA, 1988. 85(21): p. 7988–92; Ferrari, D., et al., ATP-mediated cytotoxicity in microglial cells. Neuropharmacology, 1997. 36(9): p. 1295–301; Zheng, L. M., et al., Extracellular ATP as a trigger for apoptosis or programmed cell death. J Cell Biol, 1991. 112(2): p. 279–88). Diminution of cell integrity then leads to further ATP release, propagating the inflammatory response and continued tissue destruction. Recent data have shown an attenuated effect of extracellular ATP in the presence of the regeneration and tolerance factor (RTF) protein. The present invention discloses compositions and methods to modulate inflammatory and immune responses by regulating the activities of RTF. RTF prevents ATP activation of P2Z, thus preventing the cell from undergoing pro-inflammatory activation and apoptosis.